Persons infected with HIV have been described as having alterations of adrenocortical circadian rhythms including elevated morning plasma cortisol levels, elevated 24 hour adjusted mean plasma cortisol levels, and impaired stimulated cortisol release, when these parameters are compared with values in HIV-seronegative controls. High levels of adrenocorticortical stimulating hormone (ACTH) and inappropriately normal levels of ACTH in the setting of high basal cortisol levels have also been reported in HIV-infected individuals. Evidence has been presented for the occurrence of a predictable diurnal peak of number of white blood cells, number of total T lymphocytes and percentage of helper T lymphocytes. The relationship between both endogenous glucocorticoids and exogenously administrated glucocorticoids and T lymphocyte number and subset distribution has also been described. Inferential evidence has suggested a casual and inverse relationship between cortisol levels and peak numbers of lymphocytes, peak numbers of T lymphocytes and the percentage of helper T lymphocytes. A statistically significant decrease in both the percentage and absolute number of T helper cells has been described four hours after a single dose of 20 milligrams of prednisone. In HIV-infected persons, loss of CD4 circadian rhythms has been reported, with loss of the large-amplitude, evening peaking cycle pattern. It has been suggested, however, that at least in the early stages of disease the increases described in morning serum cortisol measurements alone may not be enough to fully explain the blunting of the CD4 rhythm. Morning cortisol values by themselves, may not represent the full extent of abnormal cortisol production in abnormal individuals. Ketoconazole, an oral antifungal agent, used frequently in HIV-infected individuals for treatment of systemic candidiasis, is known to have a potent inhibitory effect on adrenal steroid production through its ability to inhibit cytochrome P450-dependent enzymes. The drug has been shown to decrease cortisol levels to normal after administration to people with Cushing's disease. In a study performed by Dr. Walser at Johns Hopkins (RPN# 90-01-11-01) in patients with chronic renal failure, mean free cortisol excretion fell 43% and mean 17-OH corticosteroid excretion fell 33% in subjects administered the combination of 400 mg of ketoconazole and 2.5 mg of prednisone daily. We hypothesize that administration of ketoconazole to people with HIV infection may decrease mean 24 hour cortisol production on a chronic basis and dampen cortisol peaks to an extent that may lead to the maintenance of T helper cell numbers at the maximal values that are physiologically possible in the setting of this disease. Therefore in this protocol we propose to study 40 HIV-infected individuals with a CD4 cell percentage equal to or greater than 15% (equivalent of approximately 200 Cell/CC3). We plan to study 20 people randomly assigned to receive 400 mg ketoconazole and 2.5 Mg prednisone daily and 20 people randomly assigned to receive placebo for eight weeks. Treatment with 2.5 mg dose of prednisone is enough to maintain physiologic glucocorticoid function in the setting of adrenal suppression by a pharmacologic agent (ketoconazole) without allowing ACTH escape. In order to assess the biological effect of this treatment on the adrenal system, we will measure levels of ACTH, and the 24 hour urinary excretion of 17-OH corticosteroids and free cortisol. Measurements will be obtained at baseline and a 2, 4, and 8 weeks of treatment. We will also measure total T cells, percentage of CD4 cells, and absolute number of CD4 cells at the same time points.